Abstract
Right ventricular (RV) failure is a common consequence of acute and chronic RV overload of pressure, such as after pulmonary embolism and pulmonary hypertension. It has been recently realized that symptomatology and survival of patients with pulmonary hypertension are essentially determined by RV function adaptation to increased afterload. Therefore, improvement of RV function and reversal of RV failure are treatment goals. Currently, the pathophysiology and the pathobiology underlying RV failure remain largely unknown. A better understanding of the pathophysiological processes involved in RV failure is needed, as there is no proven treatment for this disease at the moment. The present review aims to summarize the current understanding of the pathogenesis of RV failure, focusing on inflammation. We attempt to formally emphasize the importance of inflammation and associated representative inflammatory molecules and cells in the primum movens and development of RV failure in humans and in experimental models. We present inflammatory biomarkers and immune mediators involved in RV failure. We focus on inflammatory mediators and cells which seem to correlate with the deterioration of RV function and also explain how all these inflammatory mediators and cells might impact RV function adaptation to increased afterload. Finally, we also discuss the evidence on potential beneficial effects of targeted anti-inflammatory agents in the setting of acute and chronic RV failure.
Highlights
In the present review article, we propose an overview of the multiple players involved in the complex inflammatory response to acute or chronic increased afterload and its contribution to subsequentadaptive remodeling of the Right ventricular (RV) leading to RV dysfunction, regarding what’s already known in the left ventricle (LV) and in heart failure in general
More effort is needed to understand the mechanisms promoting this pathologic process and how to modulate it in order to develop new therapeutic interventions aiming at the reduction of RV failure and mortality in pulmonary arterial hypertension (PAH) patients
It seems that inflammation and RV failure are strongly interconnected and mutually reinforce each other
Summary
The initial insult involves the pulmonary circulation, it has been better realized recently that symptomatology and poor clinical outcome in patients with pulmonary arterial hypertension (PAH), are essentially determined by the adaptation of right ventricular (RV) function to increased afterload (Galiè et al, 2010; Vonk-Noordegraaf et al, 2013; Vonk Noordegraaf et al, 2017; Friedberg and Redington, 2014), showing the importance to consider the coupling of the RV to the pulmonary circulation, as a sole functional unit (Naeije et al, 2014). In patients with idiopathic PAH (Overbeek et al, 2008; Condliffe et al, 2009) or selected forms of congenital heart diseases, such as Eisenmenger syndrome (Kuhn et al, 2003), RV failure is less prevalent and occurs later compared to patients with PAH associated to inflammatory diseases such as systemic sclerosis (Kawut et al, 2003; Kuhn et al, 2003; Overbeek et al, 2008; Condliffe et al, 2009) In these patients, RV inflammatory infiltrates were denser than in patients with idiopathic PAH, while interstitial fibrosis was present in all the RV (Overbeek et al, 2010). In the present review article, we propose an overview of the multiple players involved in the complex inflammatory response to acute or chronic increased afterload and its contribution to subsequent (mal)adaptive remodeling of the RV leading to RV dysfunction, regarding what’s already known in the left ventricle (LV) and in heart failure in general
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